骨髓增殖性肿瘤发病机制中非恶性细胞异常的细胞因子产生及对JAK抑制剂治疗的反应。
Aberrant cytokine production by nonmalignant cells in the pathogenesis of myeloproliferative tumors and response to JAK inhibitor therapies.
作者信息
Belver Laura, Ferrando Adolfo A
机构信息
Institute for Cancer Genetics, Columbia University, New York, New York.
Institute for Cancer Genetics, Columbia University, New York, New York. Department of Pathology, Columbia University Medical Center, New York, New York. Department of Pediatrics, Columbia University Medical Center, New York, New York.
出版信息
Cancer Discov. 2015 Mar;5(3):234-6. doi: 10.1158/2159-8290.CD-15-0095.
Abstract
Kleppe and colleagues use detailed cytokine profiling analyses to investigate the role of aberrant proinflammatory cytokine secretion in the pathogenesis of myeloproliferative neoplasms. Their analyses implicate constitutive activation of STAT3 in both malignant and nonmalignant bone marrow cell populations as a driver of aberrant cytokine secretion and as a cellular target mediating the therapeutic activity of ruxolitinib.
摘要
克莱佩及其同事运用详细的细胞因子谱分析，来研究异常促炎细胞因子分泌在骨髓增殖性肿瘤发病机制中的作用。他们的分析表明，信号转导和转录激活因子3（STAT3）在恶性和非恶性骨髓细胞群体中的组成性激活，是异常细胞因子分泌的驱动因素，也是介导鲁索替尼治疗活性的细胞靶点。
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